Thromb Haemost 1999; 82(04): 1255-1259
DOI: 10.1055/s-0037-1614371
Review Article
Schattauer GmbH

A Flow Cytometric Assay of Platelet Activation Marker P-Selectin (CD62P) Distinguishes Heparin-induced Thrombocytopenia (HIT) from HIT with Thrombosis (HITT)

Wenche Jy
1   From the Wallace H. Coulter Platelet Laboratory University of Miami School of Medicine, Miami, Florida, USA
,
Wei Wei Mao
1   From the Wallace H. Coulter Platelet Laboratory University of Miami School of Medicine, Miami, Florida, USA
,
Lawrence L. Horstman
1   From the Wallace H. Coulter Platelet Laboratory University of Miami School of Medicine, Miami, Florida, USA
,
Peter A. Valant
1   From the Wallace H. Coulter Platelet Laboratory University of Miami School of Medicine, Miami, Florida, USA
,
Yeon S. Ahn
1   From the Wallace H. Coulter Platelet Laboratory University of Miami School of Medicine, Miami, Florida, USA
› Author Affiliations
Further Information

Publication History

Received 09 June 1998

Accepted after revision 17 May 1998

Publication Date:
08 December 2017 (online)

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Summary

Heparin induced thrombocytopenia (HIT) is a well-known complication of heparin administration but usually resolves upon discontinuation without sequelae. However, a small proportion of HIT patients develop thrombosis associated with HIT, designated as HITT, which is often life-threatening and may lead to gangrene and amputations. Existing laboratory methods of confirming HIT/HITT do not distinguish between HIT and HITT. We report a flow cytometric assay of platelet activation marker CD62P to distinguish the effects of addition of HIT vs. HITT plasma to normal blood. Briefly, normal whole blood was incubated with platelet-poor plasma from 12 patients with HITT, 30 with HIT, and 65 controls, in presence and absence of heparin, and expression of CD62P was assayed by flow cytometry. When the ratios of fluorescent intensity of CD62P with heparin divided by that without heparin were compared, HITT plasma induced significantly higher ratios than HIT plasma (HITT ratios ~2.5 vs. HIT ratios ~1.2; p <0.001). Eleven of 12 HITT patients were positive by this test but only 5 of 30 HIT patients were positive (p < 0.0005). In a case of HIT with silent thrombosis, this assay gave a positive results prior to clinically evident thrombosis. In conclusion, this method distinguishes HITT from HIT and may be clinically useful in the detection of HITT, allowing early intervention for preventing catastrophic thrombosis.